Why has the primary prevention of myocardial infarction in the treatment of hypertension been so elusive?

The pathogenesis of the two main killers in hypertension, myocardial infarction (MI) and stroke, differs. Prevention of strokes, about a third of which result from haemorrhage, appears more immediately responsive to the level of blood pressure (BP). MI reflects the end stage of a slow underlying atheromatous process of the coronary arteries and lowering BP can, at best, hope only to slow this process and make less likely the eventual plaque rupture and resultant occlusive thrombosis and infarction. Practically all the randomised trials have confirmed that the treatment of all grades of hypertension, down to a treated diastolic BP level of perhaps about 95 mmHg, reduces the incidence of fatal and non-fatal stroke by about 40-50%, though only two classes of antihypertensive agent i.e. diuretics (+/- other agents) and beta-blockers (+/- diuretics), have actually demonstrated this benefit. It is possible, in the elderly, that excessive lowering of systolic BP (SBP) (to below about 140 mmHg) might increase the number of deaths from stroke. Blood lipid changes which constitute coronary risk factors in untreated hypertensive patients should not be regarded in the same light if beta-blocker induced. Animal data suggest that beta-blockers inhibit catecholamine induced cardiovascular damage and modify coronary atheroma formation in the presence of stress and/or high cholesterol diets (in spite of blood lipid changes). Evidence in the moderate to severely hypertensive man also suggests that in spite of beta-blocker induced increases in blood triglyceride levels the incidence of deaths from MI markedly decreases over a ten year period in those whose SBP is well controlled.(ABSTRACT TRUNCATED AT 250 WORDS)